ArticleDiabetes2014
Gene targeting in NOD mouse embryos using zinc-finger nucleases.
Article in Diabetes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 26 citations in OpenAlex.
- Both soluble and cell surface CD137 expressed by Foxp3+ CD4 T cells restrain autoimmune diabetes.The Journal of experimental medicine · 2026Article
- Zebrafish as a Versatile Model for Cardiovascular Research: Peering into the Heart of the Matter.Cells · 2025Review
- MDA5-dependent responses contribute to autoimmune diabetes progression and hindrance.JCI insight · 2023Article
- The long and winding road: From mouse linkage studies to a novel human therapeutic pathway in type 1 diabetes.Frontiers in immunology · 2022Review
- The State-of-the-Art of Gene Editing and its Application to Viral Infections and Diseases Including COVID-19.Frontiers in cellular and infection microbiology · 2022Review
- Self-Renewing Islet TCF1Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Characterization of Type I Interferon-Associated Chemokines and Cytokines in Lacrimal Glands of Nonobese Diabetic Mice.International journal of molecular sciences · 2021Article
- UBASH3A deficiency accelerates type 1 diabetes development and enhances salivary gland inflammation in NOD mice.Scientific reports · 2020Article
- The CD137 Ligand Is Important for Type 1 Diabetes Development but Dispensable for the Homeostasis of Disease-Suppressive CD137Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Electroporation of AsCpf1/RNP at the Zygote Stage is an Efficient Genome Editing Method to Generate Knock-Out Mice Deficient in Leukemia Inhibitory Factor.Tissue engineering and regenerative medicine · 2020Article
- Interleukin-27 Is Essential for Type 1 Diabetes Development and Sjögren Syndrome-like Inflammation.Cell reports · 2019Article
- Combined congenic mapping and nuclease-based gene targeting for studying allele-specific effects of Tnfrsf9 within the Idd9.3 autoimmune diabetes locus.Scientific reports · 2019Article
- A comprehensive review on the role of co-signaling receptors and Treg homeostasis in autoimmunity and tumor immunity.Journal of autoimmunity · 2018Review
- The Role of NOD Mice in Type 1 Diabetes Research: Lessons from the Past and Recommendations for the Future.Frontiers in endocrinology · 2018Article
- CD137 Plays Both Pathogenic and Protective Roles in Type 1 Diabetes Development in NOD Mice.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- The influence of exendin-4 intervention on -obese diabetic mouse blood and the pancreatic tissue immune microenvironment.Experimental and therapeutic medicine · 2016Article
- T-cell exhaustion: understanding the interface of chronic viral and autoinflammatory diseases.Immunology and cell biology · 2016Review
- CRISPR-Cas9-Mediated Modification of the NOD Mouse Genome With Ptpn22R619W Mutation Increases Autoimmune Diabetes.Diabetes · 2016Article
- Gene editing for corneal disease management.World journal of translational medicine · 2016Article
- Increased autoimmune diabetes in pIgR-deficient NOD mice is due to a "Hitchhiking" interval that refines the genetic effect of Idd5.4.PloS one · 2015Article
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6 authors at 1 institution in 1 country.
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Abstract
Studies in NOD mice have provided important insight into the genetics and pathogenesis of type 1 diabetes (T1D). Our goal was to further explore novel methods of genetic manipulation in this mouse model. We tested the feasibility of using zinc-finger nucleases (ZFNs) to knock out a gene directly in a pure NOD background, bypassing the need of embryonic stem cells. We report here the successful application of ZFN pairs to specifically and efficiently knock out Tnfrsf9 (encoding CD137/4-1BB) directly in the NOD mouse by embryo microinjection. Histology and T1D incidence studies indicated that CD137 was dispensable for the development of insulitis but played a role to promote progression to overt diabetes in NOD mice. We also demonstrated that CD137-deficient T-cells were less diabetogenic than their wild-type counterpart when adoptively transferred into NOD.Rag1(-/-) recipients, even when CD25(+) cells were predepleted. In vitro assays suggested that CD137 deficiency had a limited effect on the suppressive function of CD4(+)CD25(+) regulatory T-cells (Tregs). Therefore, CD137 deficiency predominately affected effector T-cells rather than Tregs. Our study demonstrates the ability to generate gene-targeted knockouts in a pure NOD background by using ZFNs without potential confounding factors introduced by contaminating genetic materials obtained from other strains.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.